This patient presents a sinus node dysfunction with presence of paroxysmal, prolonged, symptomatic pauses. The total absence of atrial activity leads to the diagnosis of sinoatrial arrest and not of an atrioventricular block (the pause would have been related to blocked P waves).
Various pathophysiological mechanisms may explain the presence of this pause:
- depressed sinus automatism with an inability of the sinus node to generate one or more impulses; typically, the pause is not a multiple of the previous PP interval;
- impulse conduction abnormality and sinoatrial block, the impulse normally occurring in the sinus node but is not transmitted to the adjacent atrial myocardial cells (perisinus disease with permanent or intermittent exit block);
- vagal hypertonia; it is imperative to investigate for a triggering factor (vagal context, violent pain, fear, stress, urination, etc.) for this pause in order to differentiate patients with a genuine anatomical (fibrosis, etc) or electrophysiological (inability of sinus cells to spontaneously depolarize) sinus node dysfunction and patients with a reflex arrest occurring in a vagal context (prolongation of the spontaneous depolarization slope of the sinus cells or a sinus conduction block in conjunction with a high vagal tone) the therapeutic consequences of which differ completely.
The boundary between sinoatrial block (defect in impulse transmission) and sinus pause (absence of impulse) is difficult to establish in the absence of valid recording methods of sinus node electrical activity. This distinction becomes impossible when no P wave of sinus origin can be visualized on the electrocardiogram.
In this patient, sinus node dysfunction is likely associated with age-related idiopathic degenerative impairment amplified by the introduction of beta-blocker therapy. Cessation of this treatment did not eliminate the symptomatic episodes (lipothymia and syncopes occurring in the absence of a setting suggestive of vagal context) and a pacemaker was implanted.